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Article ; Online: Control of fetal globin expression in man: new opportunities to challenge past discoveries.

Papayannopoulou, Thalia

2020 Volume 92, Page(s) 43–50

Abstract: Decades-old findings supporting origin of F cells in adult life from adult-type progenitors and the in vitro and in vivo enhancement of fetal globin under stress conditions have been juxtaposed against recent mechanistic underpinnings. An updated ... ...

Abstract	Decades-old findings supporting origin of F cells in adult life from adult-type progenitors and the in vitro and in vivo enhancement of fetal globin under stress conditions have been juxtaposed against recent mechanistic underpinnings. An updated molecular interrogation did not debunk prior conclusions on the origin of F cells. Although fetal globin reactivation by widely diverse approaches in vitro and in response to anemic stresses in vivo is a work in progress, accumulating evidence converges toward an integrated stress response pathway. The newly uncovered developmental regulators of globin gene switching not only have provided answers to the long-awaited quest of transregulation of switching, they are also reaching a clinical threshold. Although the effect of fetal globin silencers has been robustly validated in adult cells, the response of cells at earlier developmental stages has been unclear and inadequately studied.
MeSH term(s)	Adult ; Fetal Hemoglobin/biosynthesis ; Fetal Hemoglobin/genetics ; Humans ; Silencer Elements, Transcriptional
Chemical Substances	Fetal Hemoglobin (9034-63-3)
Language	English
Publishing date	2020-10-10
Publishing country	Netherlands
Document type	Journal Article ; Review
ZDB-ID	185107-x
ISSN	1873-2399 ; 0531-5573 ; 0301-472X
ISSN (online)	1873-2399
ISSN	0531-5573 ; 0301-472X
DOI	10.1016/j.exphem.2020.09.195
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Article: The glucocorticoid receptor elicited proliferative response in human erythropoiesis is BCL11A-dependent.

Mazzarini, Maria / Cherone, Jennifer / Nguyen, Truong / Martelli, Fabrizio / Varricchio, Lilian / Funnell, Alister P W / Papayannopoulou, Thalia / Migliaccio, Anna Rita

bioRxiv : the preprint server for biology

2024

Abstract: Prior evidence indicates that the erythroid cellular response to glucocorticoids (GC) has developmental specificity, namely, that developmentally more advanced cells that are undergoing or have undergone fetal to adult globin switching are more ... ...

Abstract	Prior evidence indicates that the erythroid cellular response to glucocorticoids (GC) has developmental specificity, namely, that developmentally more advanced cells that are undergoing or have undergone fetal to adult globin switching are more responsive to GC-induced expansion. To investigate the molecular underpinnings of this, we focused on the major developmental globin regulator BCL11A. We compared:
Language	English
Publishing date	2024-02-08
Publishing country	United States
Document type	Preprint
DOI	10.1101/2024.02.05.577972
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Article ; Online: α4-Integrin deficiency in human CD34

Ulyanova, Tatyana / Cherone, Jennifer M / Sova, Pavel / Papayannopoulou, Thalia

Experimental hematology

2022 Volume 108, Page(s) 16–25

Abstract: The functional impact of integrin expression in erythropoiesis has been previously emphasized through its decisive influence on erythroid cell-microenvironment (matrix and cellular) interactions, especially under conditions of stress. Beyond that, in ... ...

Abstract	The functional impact of integrin expression in erythropoiesis has been previously emphasized through its decisive influence on erythroid cell-microenvironment (matrix and cellular) interactions, especially under conditions of stress. Beyond that, in several in vitro studies the relationship between the two erythroid integrins, α4 and α5, has been incongruous in terms of a proliferative support, either synergistic or antagonistic, whereas a dominant influence of α4 integrin on terminal erythropoiesis in vitro and in vivo has been consistently emphasized. However, the specific cellular and molecular details of this effect have not been defined, especially for human cells. In the study described here, we cultured human CD34
MeSH term(s)	Antigens, CD34/metabolism ; Cell Differentiation ; Erythroid Cells/metabolism ; Erythroid Precursor Cells/metabolism ; Erythropoiesis ; Humans ; Integrin alpha4/metabolism
Chemical Substances	Antigens, CD34 ; Integrin alpha4 (143198-26-9)
Language	English
Publishing date	2022-02-26
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	185107-x
ISSN	1873-2399 ; 0531-5573 ; 0301-472X
ISSN (online)	1873-2399
ISSN	0531-5573 ; 0301-472X
DOI	10.1016/j.exphem.2022.01.007
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Article ; Online: Patients with hypercortisolemic Cushing disease possess a distinct class of hematopoietic progenitor cells leading to erythrocytosis.

Varricchio, Lilian / Geer, Eliza B / Martelli, Fabrizio / Mazzarini, Maria / Funnell, Alister / Bieker, James J / Papayannopoulou, Thalia / Migliaccio, Anna Rita

Haematologica

2023 Volume 108, Issue 4, Page(s) 1053–1067

Abstract: Although human cell cultures stimulated with dexamethasone suggest that the glucocorticoid receptor (GR) activates stress erythropoiesis, the effects of GR activation on erythropoiesis in vivo remain poorly understood. We characterized the phenotype of a ...

Abstract	Although human cell cultures stimulated with dexamethasone suggest that the glucocorticoid receptor (GR) activates stress erythropoiesis, the effects of GR activation on erythropoiesis in vivo remain poorly understood. We characterized the phenotype of a large cohort of patients with Cushing disease, a rare condition associated with elevated cortisol levels. Results from hypercortisolemic patients with active Cushing disease were compared with those obtained from eucortisolemic patients after remission and from volunteers without the disease. Patients with active Cushing disease exhibited erythrocytosis associated with normal hemoglobin F levels. In addition, their blood contained elevated numbers of GR-induced CD163+ monocytes and a unique class of CD34+ cells expressing CD110, CD36, CD133 and the GR-target gene CXCR4. When cultured, these CD34+ cells generated similarly large numbers of immature erythroid cells in the presence and absence of dexamethasone, with raised expression of the GR-target gene GILZ. Of interest, blood from patients with Cushing disease in remission maintained high numbers of CD163+ monocytes and, although their CD34+ cells had a normal phenotype, these cells were unresponsive to added dexamethasone. Collectively, these results indicate that chronic exposure to excess glucocorticoids in vivo leads to erythrocytosis by generating erythroid progenitor cells with a constitutively active GR. Although remission rescues the erythrocytosis and the phenotype of the circulating CD34+ cells, a memory of other prior changes is maintained in remission.
MeSH term(s)	Humans ; Polycythemia/etiology ; Pituitary ACTH Hypersecretion ; Hematopoietic Stem Cells/metabolism ; Glucocorticoids/pharmacology ; Receptors, Glucocorticoid/genetics ; Receptors, Glucocorticoid/metabolism ; Dexamethasone/pharmacology ; Cells, Cultured
Chemical Substances	Glucocorticoids ; Receptors, Glucocorticoid ; Dexamethasone (7S5I7G3JQL)
Language	English
Publishing date	2023-04-01
Publishing country	Italy
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2333-4
ISSN	1592-8721 ; 0017-6567 ; 0390-6078
ISSN (online)	1592-8721
ISSN	0017-6567 ; 0390-6078
DOI	10.3324/haematol.2021.280542
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Article ; Online: CD4

Benkhoucha, Mahdia / Tran, Ngoc Lan / Breville, Gautier / Senoner, Isis / Bradfield, Paul F / Papayannopoulou, Thalia / Merkler, Doron / Korn, Thomas / Lalive, Patrice H

Journal of neuroinflammation

2022 Volume 19, Issue 1, Page(s) 103

Abstract: Objective: c-Met, a tyrosine kinase receptor, is the unique receptor for hepatocyte growth factor (HGF). The HGF/c-Met axis is reported to modulate cell migration, maturation, cytokine production, and antigen presentation. Here, we report that CD4: ... ...

Abstract	Objective: c-Met, a tyrosine kinase receptor, is the unique receptor for hepatocyte growth factor (HGF). The HGF/c-Met axis is reported to modulate cell migration, maturation, cytokine production, and antigen presentation. Here, we report that CD4 Methods: c-Met expression by CD4 Results: CD4
MeSH term(s)	Animals ; Encephalomyelitis, Autoimmune, Experimental/pathology ; Humans ; Integrin alpha4 ; Mice ; Mice, Inbred C57BL ; Multiple Sclerosis/pathology ; Neuroinflammatory Diseases ; Th17 Cells
Chemical Substances	Integrin alpha4 (143198-26-9)
Language	English
Publishing date	2022-04-29
Publishing country	England
Document type	Journal Article
ZDB-ID	2156455-3
ISSN	1742-2094 ; 1742-2094
ISSN (online)	1742-2094
ISSN	1742-2094
DOI	10.1186/s12974-022-02461-7
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Article ; Online: Reappraising the role of α5 integrin and the microenvironmental support in stress erythropoiesis.

Ulyanova, Tatyana / Georgolopoulos, Grigorios / Papayannopoulou, Thalia

Experimental hematology

2019 Volume 81, Page(s) 16–31.e4

Abstract: We previously studied the role of β1 integrin and some of its different α partners relevant to erythropoiesis. Although clear and consistent answers regarding the role of α4β1 (VLA-4) were evident, the role of its companion integrin α5β1 (VLA-5) was ... ...

Abstract	We previously studied the role of β1 integrin and some of its different α partners relevant to erythropoiesis. Although clear and consistent answers regarding the role of α4β1 (VLA-4) were evident, the role of its companion integrin α5β1 (VLA-5) was clouded by inconsistent outcomes in all prior publications. Furthermore, the functional consequences of integrin deficiencies only in microenvironmental (ME) cells supporting erythroid cell expansion and maturation post stress have never been explored. In the study described here, we created several additional mouse models in the aim of addressing unanswered questions regarding functional consequences of single or combined integrin deficiencies in erythroid cells or only in ME supporting cells. Our novel and expansive data solidified the intrinsic requirement of both α4 and α5 integrins in erythroid cells for their proliferative expansion and maturation in response to stress; α5 integrin alone, deleted either early in all hematopoietic cells or only in erythroid cell, has only a redundant role in proliferative expansion and is dispensable for erythroid maturation. By contrast, α4 integrin, on its own, exerts a dominant effect on timely and optimal erythroid maturation. Deficiency of both α4 and α5 integrins in ME cells, including macrophages, does not negatively influence stress response by normal erythroid cells, in great contrast to the effect of ME cells deficient in all β1 integrins. Collectively the present data offer deeper insight into the coordination of different β1 integrin functional activities in erythroid cells or in ME cells for optimal erythroid stress response.
MeSH term(s)	Animals ; Erythroid Cells/cytology ; Erythroid Cells/metabolism ; Erythropoiesis ; Integrin alpha4beta1/genetics ; Integrin alpha4beta1/metabolism ; Integrin alpha5/genetics ; Integrin alpha5/metabolism ; Integrin alpha5beta1/genetics ; Integrin alpha5beta1/metabolism ; Integrin beta1/genetics ; Integrin beta1/metabolism ; Macrophages/cytology ; Macrophages/metabolism ; Mice ; Mice, Knockout ; Stem Cell Niche ; Stress, Physiological
Chemical Substances	Integrin alpha4beta1 ; Integrin alpha5 ; Integrin alpha5beta1 ; Integrin beta1 ; Itgb1 protein, mouse
Language	English
Publishing date	2019-12-28
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	185107-x
ISSN	1873-2399 ; 0531-5573 ; 0301-472X
ISSN (online)	1873-2399
ISSN	0531-5573 ; 0301-472X
DOI	10.1016/j.exphem.2019.12.004
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Article ; Online: Myocardial Infarction Does Not Accelerate Atherosclerosis in a Mouse Model of Type 1 Diabetes.

Kramer, Farah / Martinson, Amy M / Papayannopoulou, Thalia / Kanter, Jenny E

Diabetes

2020 Volume 69, Issue 10, Page(s) 2133–2143

Abstract: In addition to increasing the risk of an initial myocardial infarction (MI), diabetes increases the risk of a recurrent MI. Previous work suggests that an experimental MI can accelerate atherosclerosis via monocytosis. To test whether diabetes and ... ...

Abstract	In addition to increasing the risk of an initial myocardial infarction (MI), diabetes increases the risk of a recurrent MI. Previous work suggests that an experimental MI can accelerate atherosclerosis via monocytosis. To test whether diabetes and experimental MI synergize to accelerate atherosclerosis, we performed ligation of the left anterior descending coronary artery to induce experimental MI or sham surgery in nondiabetic and diabetic mice with preexisting atherosclerosis. All mice subjected to experimental MI had significantly reduced left ventricular function. In our model, in comparisons with nondiabetic sham mice, neither diabetes nor MI resulted in monocytosis. Neither diabetes nor MI led to increased atherosclerotic lesion size, but diabetes accelerated lesion progression, exemplified by necrotic core expansion. The necrotic core expansion was dependent on monocyte recruitment, as mice with myeloid cells deficient in the adhesion molecule integrin α4 were protected from necrotic core expansion. In summary, diabetes, but not MI, accelerates lesion progression, suggesting that the increased risk of recurrent MI in diabetes is due to a higher lesional burden and/or elevated risk factors rather than the acceleration of the underlying pathology from a previous MI.
MeSH term(s)	Animals ; Atherosclerosis/metabolism ; Atherosclerosis/pathology ; Cell Adhesion/physiology ; Diabetes Mellitus, Experimental/metabolism ; Diabetes Mellitus, Experimental/pathology ; Diabetes Mellitus, Type 1/metabolism ; Diabetes Mellitus, Type 1/pathology ; Echocardiography ; Female ; Lipid Metabolism/physiology ; Male ; Mice ; Mice, Inbred C57BL ; Monocytes/cytology ; Myocardial Infarction/metabolism ; Myocardial Infarction/pathology ; Real-Time Polymerase Chain Reaction
Language	English
Publishing date	2020-07-21
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	80085-5
ISSN	1939-327X ; 0012-1797
ISSN (online)	1939-327X
ISSN	0012-1797
DOI	10.2337/db20-0152
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Article ; Online: Evolving insights into the synergy between erythropoietin and thrombopoietin and the bipotent erythroid/megakaryocytic progenitor cell.

Papayannopoulou, Thalia / Kaushansky, Kenneth

Experimental hematology

2016 Volume 44, Issue 8, Page(s) 664–668

Abstract: ... in Experimental Hematology (Papayannopoulou T, Brice M, Farrer D, Kaushansky K. Exp Hematol. 1996;24:660-669) and ...

Abstract	Although the synergy between erythropoietin and thrombopoietin has previously been pointed out, the clonal demonstration of a human bipotent erythroid/megakaryocytic progenitor (MEP) was first published in Experimental Hematology (Papayannopoulou T, Brice M, Farrer D, Kaushansky K. Exp Hematol. 1996;24:660-669) and later in the same year in Blood (Debili N, Coulombel L, Croisille L, et al. Blood. 1996;88:1284-1296). This demonstration, and the fact that both bipotent and monopotent erythroid or megakaryocytic progenitors co-express markers of both lineages and respond to both lineage-specific transcription factors, has provided a background for the extensive use of MEP assessment by fluorescence-activated cell sorting in many subsequent studies. Beyond this, the demonstration of shared regulatory elements and the presence of single mutations affecting both lineages have inspired further studies to decipher how the shift in transcription factor networks occurs from one lineage to the other. Furthermore, in addition to shared effects, erythropoietin and thrombopoietin have additional independent effects. Most notable for thrombopoietin is its effect on hematopoietic stem cells illustrated by in vitro and in vivo approaches.
MeSH term(s)	Animals ; Biomarkers ; Cell Differentiation ; Cell Lineage ; Erythroid Precursor Cells/cytology ; Erythroid Precursor Cells/drug effects ; Erythroid Precursor Cells/physiology ; Erythropoietin/pharmacology ; Erythropoietin/physiology ; Humans ; Megakaryocyte Progenitor Cells/cytology ; Megakaryocyte Progenitor Cells/drug effects ; Megakaryocyte Progenitor Cells/physiology ; Phenotype ; Thrombopoietin/pharmacology ; Thrombopoietin/physiology
Chemical Substances	Biomarkers ; Erythropoietin (11096-26-7) ; Thrombopoietin (9014-42-0)
Language	English
Publishing date	2016-08
Publishing country	Netherlands
Document type	Journal Article ; Review
ZDB-ID	185107-x
ISSN	1873-2399 ; 0531-5573 ; 0301-472X
ISSN (online)	1873-2399
ISSN	0531-5573 ; 0301-472X
DOI	10.1016/j.exphem.2015.11.010
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Article: HDAd5/35

Li, Chang / Psatha, Nikoletta / Gil, Sucheol / Wang, Hongjie / Papayannopoulou, Thalia / Lieber, André

Molecular therapy. Methods & clinical development

2018 Volume 9, Page(s) 390–401

Abstract: We generated helper-dependent HDAd5/ ... ...

Abstract	We generated helper-dependent HDAd5/35
Language	English
Publishing date	2018-05-01
Publishing country	United States
Document type	Journal Article
ZDB-ID	2872938-9
ISSN	2329-0501 ; 2329-0501
ISSN (online)	2329-0501
ISSN	2329-0501
DOI	10.1016/j.omtm.2018.04.008
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Article: Brief Report: A Differential Transcriptomic Profile of Ex Vivo Expanded Adult Human Hematopoietic Stem Cells Empowers Them for Engraftment Better than Their Surface Phenotype.

Psatha, Nikoletta / Georgolopoulos, Grigorios / Phelps, Susan / Papayannopoulou, Thalia

Stem cells translational medicine

2017 Volume 6, Issue 10, Page(s) 1852–1858

Abstract: Transplantation of small cord blood (CB) units, or of autologous ex vivo-genetically modified adult hematopoietic stem cells (HSC), face the common challenge of suboptimal HSC doses for infusion and impaired engraftment of the transplanted cells. Ex vivo ...

Abstract	Transplantation of small cord blood (CB) units, or of autologous ex vivo-genetically modified adult hematopoietic stem cells (HSC), face the common challenge of suboptimal HSC doses for infusion and impaired engraftment of the transplanted cells. Ex vivo expansion of HSCs, using either cell-based coculture approaches or especially small molecules have been successfully tested mainly in CB and in prolonged cultures. Here, we explored whether innovative combinations of small molecules can sufficiently, after short culture, expand adult HSCs while retaining their functionality in vivo. We found that 5-day cultured cells, in the presence of the small molecule combinations tested, achieved higher engraftment levels in NSG mice than both their uncultured and their cytokine only-cultured counterparts. Surprisingly, the engraftment levels were neither concordant to the numbers of phenotypically similar HSCs expanded under different small molecule combinations, nor explained by their distinct companion cells present. Transcriptomic comparative analysis of sorted, phenotypically similar, ex vivo generated HSCs transplanted in equal numbers, suggested that HSCs generated under expansion conditions that maintain low expression of the Rap1/Ras/PI3K-AKT pathway exhibit a superior functional profile in vivo. Stem Cells Translational Medicine 2017;6:1852-1858.
MeSH term(s)	Animals ; Cells, Cultured ; Hematopoietic Stem Cell Transplantation/methods ; Hematopoietic Stem Cells/cytology ; Hematopoietic Stem Cells/drug effects ; Hematopoietic Stem Cells/metabolism ; Humans ; Imidazoles/pharmacology ; Indoles/pharmacology ; Mice ; Phenotype ; Purines/pharmacology ; Pyridines/pharmacology ; Pyrimidines/pharmacology ; Transcriptome
Chemical Substances	Imidazoles ; Indoles ; Purines ; Pyridines ; Pyrimidines ; StemRegenin 1 ; UM171 compound ; ralimetinib (73I34XW4HD)
Language	English
Publishing date	2017-08-11
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2642270-0
ISSN	2157-6580 ; 2157-6564
ISSN (online)	2157-6580
ISSN	2157-6564
DOI	10.1002/sctm.17-0048
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